When a pharmaceutical company changes an SPC or PIL, a new version is published on medicines.ie. For each version, we show the dates it was published on medicines.ie and the reasons for change.
Atenolol may mask the signs of thyrotoxicosis.
In hypertensive patients, there is evidence that beta-blockers, including atenolol, may affect glucose metabolism and may be associated with the development of diabetes.
Adrenergic neurone-blocking agents
Adrenergic neurone-blocking agents such as guanethidine, reserpine, diuretics and antihypertensive agents, including the vasodilator group, will have an addictive effect on the hypotensive action of the drug.
Anaesthetic agents
Caution must be exercised when using anaesthetic agents with Ateni. The anaesthetist should be informed and the choice of anaesthetic should be an agent with as little negative inotropic activity as possible. Use of beta-blockers with anaesthetic drugs may result in attenuation of the reflex tachycardia and increase the risk of hypotension. Anaesthetic agents causing myocardial depression are best avoided.
Antiarrhythmic agents (Class 1)
Caution must be exercised when prescribing a beta-blocker with Class 1 antiarrhythmic agents such as disopyramide.
Calcium channel blockers
Combined use of beta-blockers and calcium channel blockers with negative inotropic effects, e.g. verapamil or diltiazem, can lead to an exaggeration of these effects particularly in patients with impaired ventricular function and/or sinoatrial or atrioventricular conduction abnormalities. This may result in severe hypotension, bradycardia and cardiac failure. Neither the beta-blocker nor the calcium channel blocker should be administered intravenously within 48 hours of discontinuing the other.
Clonidine
Beta-blockers may exacerbate the rebound hypertension, which can follow the withdrawal of clonidine. If the two drugs are co-administered, the beta-blocker should be withdrawn several days before discontinuing clonidine. If replacing clonidine by beta-blocker therapy, the introduction of beta-blockers should be delayed for several days after clonidine administration has stopped.
Digitalis glycosides
Digitalis glycosides, in association with beta-blockers, may increase atrioventricular conduction time.
Dihydropyridines
Concomitant therapy with dihydropyridines, e.g. nifedipine, may increase the risk of hypotension, and cardiac failure may occur in patients with latent cardiac insufficiency.
Insulin and oral antidiabetic drugs
Concomitant use with insulin and oral antidiabetic drugs may lead to the intensification of the blood sugar lowering effects of these drugs. Symptoms of hypoglycaemia, particularly tachycardia, may be masked (See Section 4.4).
Myocardial depressants
The beta-blocker should only be used with caution in patients who are receiving concomitant myocardial depressants such as halogenated anaesthetics, lidocaine, procainamide and beta-adrenoceptor stimulants such as noradrenaline (norepinephrine).
Prostaglandin synthetase-inhibiting drugs
Concomitant use of prostaglandin synthetase-inhibiting drugs, e.g. ibuprofen, indometacin, may decrease the hypotensive effects of beta-blockers.
Sympathomimetic agents
Concomitant use of sympathomimetic agents, e.g. adrenaline (epinephrine), may counteract the effect of beta-blockers.
Barbituric acid derivatives
Concomitant use of derivatives of barbituric acid should be avoided.
Cimetidine
Other anti-hypertensive agents will potentiate the hypotensive action of atenolol.
Parental administration of preparations containing adrenaline to patients taking beta-adrenoceptor blocking drugs may, in rare cases, result in vasoconstriction, hypertension and bradycardia.
Beta-adrenoceptor blocking drugs may enhance the negative inotropic and chronotropic actions of verapamil. Therefore, concurrent use requires great care. The negative inotropic effects of class I anti-dysrhythmic agents such as disopyramide and certain anaesthetics may also be enhanced by beta-blocking drugs.
Beta-adrenoceptor blocking drugs can exacerbate the rebound hypertension associated with sudden withdrawal of clonidine.
Beta-blockers may enhance hypoglycaemic effects of anti-diabetic agents and mask the warning signs of hypoglycaemia such as tremor and tachycardia.
Co-administration with an NSAID such as indomethacin or ibuprofen may lead to a decrease in the hypotensive effect of atenolol.
Concurrent administration with a cardiac glycoside may lead to an increase in atrio-ventricular conduction time.
Combined use of beta-blocking drugs and calcium channel blockers with negative inotropic effects eg verapamil, diltiazem can lead to an exaggeration of these effects, particularly in patients with impaired ventricular function and/or sino-atrial or atrio-ventricular conduction abnormalities. Co-administartion of beta-blockers with cimetidine or hydralazine can increase the effect of beta-blockers.
Ateni tablets are well tolerated. In clinical studies, the undesired effects reported are usually attributable to the pharmacological actions of atenolol.
The following undesired events, listed by body system, have been reported with the following frequencies: very common (≥ 10%), common (1-9.9%), uncommon (0.1-0.9%), rare (0.01-0.09%), very rare (< 0.01%) including isolated reports.
Cardiac disorders:
Common: Bradycardia.
Rare: Heart failure deterioration, precipitation of heart block.
Vascular disorders:
Common: Cold extremities.
Rare: Postural hypotension, which may be associated with syncope, intermittent claudication may be increased if already present, in susceptible patients Raynaud’s phenomenon.
Nervous system disorders:
Rare: Dizziness, headache, paraesthesia.
Psychiatric disorders:
Uncommon: Sleep disturbances of the type noted with other beta-blockers.
Rare: Mood changes, nightmares, confusion, psychoses and hallucinations.
Gastrointestinal disorders:
Common: Gastrointestinal disturbances.
Rare: Dry mouth.
Investigations:
Uncommon: Elevations of transaminase levels.
Very rare: An increase in ANA (Antinuclear Antibodies) has been observed, however the clinical relevance of this is not clear.
Hepato-biliary disorders:
Rare: Hepatic toxicity including intrahepatic cholestasis.
Blood and lymphatic system disorders:
Rare: Purpura, thrombocytopenia.
Skin and subcutaneous tissue disorders:
Rare: Alopecia, psoriasiform skin reactions, exacerbation of psoriasis, skin rashes.
Eye disorders:
Rare: Dry eyes, visual disturbances.
Reproductive system and breast disorders:
Rare: Impotence.
Respiratory, thoracic and mediastinal disorders:
Rare: Bronchospasm may occur in patients with bronchial asthma or a history of asthmatic complaints.
General disorders and administration site conditions:
Common: Fatigue.
In clinical studies, the side effects reported are usually attributable to its pharmacological actions and include coldness of the extremities, muscular fatigue and, in isolated cases, bradycardia. Bradycardia and hypotension are usually a sign of overdosage, but may rarely be due to intolerance of the drug. Sleep disturbances of the type noted with other beta-blockers.
Atenolol is generally well tolerated. Other side effects include nausea, vomiting, dry mouth, diarrhoea, postural hypotension, confusion, dizziness, nightmares and lassitude. Headache, mood changes, psychoses, hallucinations and deterioration in heart failure may occur occasionally. Rarely thrombocytopenia, alopecia, purpura, psoriasis form skin reactions and exacerbation of psoriasis.
Precipitation of heart block, intermittent claudication and Raynaud’s phenomenon in susceptible patients have been reported.
Other side effects include paraesthesia and eyesight changes. Bronchospasm may occur in patients with bronchial asthma or a history of allergic disease.
May mask the signs of thyrotoxicosis.
An increase in ANA (anti nuclear antibodies) has been observed, however the clinical relevance of this is not clear.
There have been reports of skin rashes and/or dry eyes associated with the use of beta-adrenergic blocking drugs. The reported incidence is small and in most cases the symptoms have cleared when treatment was withdrawn.
The symptoms of overdosage may include bradycardia, hypotension, acute cardiac insufficiency and bronchospasm.
Treatment:
If required, gastric emptying and charcoal. Important note! Atropine should be given before gastric emptying (due to the risk of stimulation of the vagus). Intubation and treatment with respirator should be considered. Adequate fluid substitution, infusion of glucose and ECG-supervision should be considered. Eventually the dose of atropine may need to be repeated to prevent vagal symptoms.
Clinical features of overdosage may include bradycardia, hypotension, bronchospasm, hypoglycaemia, delirium and unconsciousness. Following recent overdosage, the stomach should be emptied by gastric aspiration and lavage.
Severe bradycardia may respond to atropine 1 to 2 mg intravenously. If necessary, this may be followed by a bolus dose of glucagon 5 to 10 mg intravenously, followed if necessary be y an intravenous infusion of glucagon 1 to 5 mg per hour or more according to response. If there is no response to glucagons, or if glucagon is unavailable, a beta-adrenoceptor stimulant such as dobutamine 2.5-10 mcg/kg/minute by intravenous infusion or isoprenaline 10-25 mcg given as an infusion at a rate not exceeding 5 mcg/minute may be given. Occasionaly a temporary pacing wire may be required. Atenolol is dialysable.
Pharmacotherapeutic group: beta-blocking agents, selective; ATC Code: C07A B03.